• 1 January 1977
    • journal article
    • research article
    • Vol. 201  (2) , 406-415
Abstract
Propranolol markedly increased the norepinephrine-induced maximal force in circular smooth muscle of the rat portal, mesenteric, renal and, to a lesser extent, femoral veins without affecting aortic or mesenteric artery responses to norepinephrine. Furthermore, 2 other .beta.-receptor antagonists, practolol and N-isopropylmethoxamine, specifically enhanced maximal venous responses to norepinephrine. Contractions to norepinephrine, but not to serotonin, were increased by propranolol only in veins, even after the vasodilator, papaverine. The ability of propranolol to enhance norepinephrine-induced contraction in these rat veins paralleled the effectiveness of isoproterenol to relax such tissues. .beta.-Receptor antagonists enhanced the response of veins to the field stimulated release of norepinephrine from sympathetic nerves. .beta.-Adrenergic stimulation appears to modulate norepinephrine-induced constriction in certain rat veins but not in the aorta or mesenteric artery.